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  4. There’s a patient that presents with a facetious hyperthyroid state because of too much thyroid medication, and Chris is saying that the patient has levels of cortisol that are too high but low levels of cortisone. I thought that when patients had hyperthyroid states they usually presented with the opposite. I’m confused. I think I understood the physiology that would make more sense. He states that oftentimes people with hyperthyroidism have troubles converting cortisol to cortisone, but he also said in the earlier cortisol/cortisone slide that patients with hyperthyroidism often present with high cortisone levels, so I don’t understand.

There’s a patient that presents with a facetious hyperthyroid state because of too much thyroid medication, and Chris is saying that the patient has levels of cortisol that are too high but low levels of cortisone. I thought that when patients had hyperthyroid states they usually presented with the opposite. I’m confused. I think I understood the physiology that would make more sense. He states that oftentimes people with hyperthyroidism have troubles converting cortisol to cortisone, but he also said in the earlier cortisol/cortisone slide that patients with hyperthyroidism often present with high cortisone levels, so I don’t understand.

Chris Kresser:  Well, it is all very confusing. I think, as a general comment, you have to remember that there’s a textbook presentation and then there’s the reality of what we see in clinical practice. Sometimes they match and sometimes they don’t. I’m sure, Leslie and anyone else who’s listening, if you’ve been in practice for some time, you know that. And this manifests not only in the case of the HPA axis panels, but in just about any other situation. I’m working on the thyroid content right now, and the textbook says that in hypothyroidism, patients should have a high TSH and low T4 and T3, but of course, we don’t always see that. Sometimes we see patients with low T4 and low T3 and low TSH. That’s a whole different situation, and we’ll be talking about that. Other times, patients have high T4 and T3, but their TSH is still a little bit high, so what do we make of that? These are the situations that we don’t find in the textbook. So you have to put all the various pieces together and just make a clinical judgment call, and if one of the pieces doesn’t make sense, but all of the other pieces do, plus the symptoms match with all the other pieces, then I would tend to give that one piece that doesn’t fit less weight and not necessarily disregard it entirely, but it wouldn’t probably affect or change my treatment plan in that particular situation. It’s similar to the previous question in the sense that we’re kind of assembling a number of different pieces of information to build a clinical diagnosis. Ultimately the diagnosis is clinical. It’s not dependent on any one particular piece of information except in rare circumstances.

 

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